Side-by-side · Research reference

BronchogenvsFollistatin-344

Side-by-side comparison across mechanism, dosage, evidence, side effects, administration, and stack synergies. Citations on every claim where available.

AAnimal-StrongHUMAN-REVIEWED16/35 cited

BHuman-MechanisticHUMAN-REVIEWED4/58 cited

Bronchogen

Tetrapeptide Bioregulator · Khavinson-School

0.05 ng/mLEffective concentrationZakutskiĭ 2006

60 daysCOPD model durationTitova 2017

30 daysTreatment courseKuzubova 2015

Research models: tissue culture / parenteral

Follistatin-344

Myostatin/Activin Antagonist · Research Use

15–25%FST/MSTN ratio ↑

344 AACirculating isoform

ResearchPhase status

Research · No approved protocol

01Mechanism of Action

Parameter

Bronchogen

Follistatin-344

Primary target

Bronchial epithelial cellsKuzubova 2015

Myostatin (MSTN/GDF-8) and Activin A

Pathway

Tissue-specific bioregulation → epithelial cell differentiation → ciliated cell restoration

FST-344 binds MSTN/Activin → prevents ActRIIB receptor engagement → disinhibits muscle anabolism

Downstream effect

Reversal of goblet cell hyperplasia, squamous metaplasia elimination, restoration of ciliated epithelium, normalized secretory IgA and surfactant protein B productionKuzubova 2015 Titova 2017

Elevated follistatin/myostatin ratio, increased muscle protein synthesis, attenuated muscle atrophy signalingJeong 2026

Feedback intact?

—

Yes — indirect antagonist, preserves endogenous regulation

Origin

Synthetic tetrapeptide (Ala-Glu-Asp-Leu) from Khavinson bioregulator framework

Endogenous glycoprotein, 344-AA isoform lacking heparin-binding domain (vs FST-315)

Antibody development

—

Not documented in available trials (endogenous protein)

02Dosage Protocols

Parameter

Bronchogen

Follistatin-344

Effective concentration (culture)

0.05 ng/mLZakutskiĭ 2006

Demonstrated in organotypic tissue culture of bronchial explants.

—

Treatment duration (animal)

1 month (30 days)Kuzubova 2015 Titova 2017

Course duration in rat COPD models.

—

Evidence basis

Animal models (rat) / organotypic cultureTitova 2017 Kuzubova 2015 Zakutskiĭ 2006

No human clinical trials reported in available literature.

Human observational / biomarker studies

Model system

NO₂-induced COPD (60-day intermittent exposure)Titova 2017

—

Tissue specificity

Selective for bronchopulmonary tissue

Part of Khavinson organ-specific bioregulator series.

—

Clinical protocol

—

None — no approved dosing regimen

Follistatin-344 measured as endogenous biomarker, not administered exogenously in cited trials.

Research context

—

Endogenous modulation via exercise + nutrition

Resistance training + EAA intake elevated FST/MSTN ratio by 15–25% in 12-week RCT (older women).

Half-life

—

Not established

Circulating isoform; lacks tissue-binding domain of FST-315.

03Metabolic / Fat Loss Evidence

Parameter

Bronchogen

Follistatin-344

Primary target

—

Muscle mass preservation, not direct lipolysis

Indirect fat effect

—

Increased lean mass → elevated resting metabolic rate

Not primary mechanism. Muscle-sparing during deficit.

Clinical evidence

—

Lorcaserin trial (6 mo) showed no MAFI axis changes during fat lossRamirez-Cisneros 2026

Suggests follistatin not primary driver of fat loss in weight-reduction interventions.

GLP-1RA studies

—

Liraglutide (35 days) — no significant MAFI axis modulation despite fat/lean changes

04Side Effects & Safety

Parameter

Bronchogen

Follistatin-344

Animal safety profile

No adverse effects reported in published rat studies

Limited safety data; only animal models available.

—

Human data

Absent — no clinical trials in humans reported

—

Long-term effects

Unknown — maximum study duration 30 days in animals

—

Clinical safety data

—

None — no human exogenous administration trials in literature

Theoretical risks

—

Excessive myostatin inhibition → muscle overgrowth, impaired glucose tolerance

Based on myostatin-null animal models and clinical myostatin inhibitor trials.

Endogenous elevation (exercise)

—

No adverse effects reported in 12-week resistance + EAA trials

Cancer risk (theoretical)

—

Myostatin inhibition may promote tumor growth in malignancy (preclinical data)

Regulatory status

—

Not approved for human use — research peptide only

Absolute Contraindications

Bronchogen

—

Follistatin-344

·Active malignancy
·No approved protocol — research use only

Relative Contraindications

Bronchogen

—

Follistatin-344

·Insulin resistance / Type 2 diabetes (monitor glucose)
·Pregnancy / lactation (unknown safety profile)

05Administration Protocol

Parameter

Bronchogen

Follistatin-344

1. Research context only

Bronchogen has been studied exclusively in animal models and organotypic tissue culture. No approved formulation or human administration protocol exists.

Follistatin-344 is not approved for human administration. All cited studies measure endogenous serum follistatin as a biomarker, not as an exogenous therapeutic agent.

2. Animal model protocol

In rat COPD models, tetrapeptide administered for 30-day course following 60-day NO₂ exposure. Route and exact dosing not specified in abstracts.Titova 2017 Kuzubova 2015

Resistance exercise combined with essential amino acid (EAA) supplementation elevated the follistatin/myostatin ratio by 15–25% in 12-week randomized trials. Protein intake (1.2–1.5 g/kg/day) synergizes with training to upregulate endogenous follistatin.

3. Organotypic culture

Bronchial tissue explants from young (3-week) and aged (18-month) rats cultured in medium containing 0.05 ng/mL bronchogen, demonstrating tissue-specific stimulation.Zakutskiĭ 2006

Serum follistatin and follistatin/myostatin ratio are used diagnostically in sarcopenia screening and as biomarkers of muscle anabolic balance in clinical trials.

4. Khavinson bioregulator tradition

Part of Russian peptide bioregulator framework emphasizing tissue-specific low-dose effects. Typically administered parenterally in related peptides from this series.

Gene therapy and recombinant follistatin delivery are under preclinical investigation for muscular dystrophy and sarcopenia. No human safety or efficacy data for exogenous FST-344 administration.

06Stack Synergy

Bronchogen

— no documented stacks

Follistatin-344

+ BPC-157

Multi-pathway

View BPC-157 →

Follistatin-344 (myostatin antagonist) and BPC-157 (tissue repair peptide) address complementary pathways in muscle recovery. FST-344 promotes muscle protein synthesis by disinhibiting myostatin signaling, while BPC-157 accelerates healing of tendons, ligaments, and microtears via angiogenesis and collagen synthesis. Combined, they may support both hypertrophy and structural repair during high-volume training or injury recovery.

Follistatin-344: No approved protocol — endogenous modulation via resistance exercise + EAA
BPC-157: 250–500 mcg SQ · twice daily · near injury site or systemic
Duration: 4–8 weeks
Primary benefit: Muscle hypertrophy + accelerated soft tissue repair

+ TB-500

Moderate

View TB-500 →

TB-500 (thymosin beta-4 fragment) promotes cell migration, angiogenesis, and anti-inflammatory signaling in muscle and connective tissue. Follistatin-344's anabolic signaling may synergize with TB-500's regenerative effects during muscle damage or overtraining, particularly in older adults where both myostatin inhibition and tissue repair are rate-limiting.

Follistatin-344: Endogenous upregulation (resistance training + protein)
TB-500: 2–5 mg SQ · twice weekly · loading phase 4 weeks, then maintenance
Frequency: Twice weekly TB-500, daily training stimulus for FST
Primary benefit: Enhanced recovery, reduced inflammation, muscle growth support